1. Field of the Invention
This invention relates to injection catheters and, more particularly, to a novel subcutaneous peritoneal injection catheter apparatus and method for providing injection access to the peritoneal cavity.
2. The Prior Art
Glucose is a major fuel for the body with the brain being the notable consumer. Insulin is required by many, but not all, tissues for the uptake and/or utilization of glucose.
The liver and pancreas are the pivotal organs in glucose control with insulin serving as a vital regulatory hormone. For example, in response to rising levels of glucose, the pancreatic beta cells secrete insulin which travels from the pancreas to the portal vein and then to the liver where the liver extracts approximately 50 percent of the insulin. The remaining 50% of the insulin then travels throughout the rest of the body to specific receptors in other tissues. In response to insulin, the liver commences storage of glucose in the form of glycogen (a starch). In the fasting state, the liver releases a steady output of this stored glucose thereby supplying many body tissues with their requisite amounts of glucose.
Conversely glucose utilization by other tissues is insignificantly affected by normal pancreatic insulin secretion. It has been stated that the greater response of the liver as compared to peripheral tissues (fat and muscle) to small changes in insulin levels need not reflect an inherently greater sensitivity on the part of the liver cell (hepatocyte), rather, it may be a consequence of high ambient levels of endogenous (self-produced) insulin in portal as compared to peripheral blood. In summary, therefore, the major effect of insulin in a normal human is to lower the blood glucose levels by decreasing the rate of glucose output by the liver.
Diabetics suffer from relative or absolute deficiency in insulin secretion (resulting in high blood sugar levels) and tissue cells which are "starving" for glucose yet are unable to "feed" (absorb glucose) in the absence of insulin. Historically, the treatment has been to provide insulin by injections into the peripheral circulation either from a subcutaneous depot or as an intravenous slow infusion. The result is that only about 10 percent of the administered dose of insulin reaches the liver as compared to approximately 50 percent in normal persons. As a consequence, hepatic glucose production is not first reduced; rather, blood glucose is lowered by increased utilization by other tissues (muscle, fat) as a result of the presence of high levels of insulin in the peripheral circulation. Accordingly, normal levels of blood sugar are achieved only by carefully matching any increased peripheral utilization of blood sugar to an increased hepatic production, which is inherently much more difficult than simply decreasing hepatic glucose production.
When demand for blood sugar exceeds the supply (as a result of too much insulin injected), the blood glucose drops below normal values. There is little glucose reserve since the liver, in its state of under-insulinization, is already releasing glucose. The result is that the blood sugar level will plummet despite adequate levels of counterregulatory hormones (glucagon, epinephine, norepinephine, and growth hormone) whose actions are to increase liver production of glucose in emergency situations. This hypoglycemic reaction, a progression of symptoms from nervousness, sweating, stupor, unconsciousness, and occasionally, irreparable brain damage, will occur until sugary substances are taken by mouth or intravenously.
The ongoing cycle between hyperglycemia and hypoglycemia has created a basic rift in the philosophy of diabetic control. The "tight control" philosophy claims that the long-term devastations of diabetes (blindness, heart attacks, kidney failure, and loss of extremities) are due to abnormally elevated sugar levels, and strives to keep blood sugar within the normal range even at the risk of frequent (more than once a week) hypoglycemic reactions. The converse of the foregoing is the "loose control" philosophy which is based on the presumption that the basic foundation of the tight control philosophy has yet to be proved and that the considerable risks of hypoglycemic reactions are not worth an unproved benefit.
The intraperitoneal delivery of insulin has recently been investigated as an alternative to both the intravenous and subcutaneous delivery sites. Although access to the intraperitoneal site is more difficult, it has the potential advantages of avoiding peripheral hyperinsulinaemia (high blood insulin levels), insulinizing the liver via direct portal venous system insulin absorption, and more rapid absorption than subcutaneously delivered insulin. Preliminary results appear favorable for intraperitoneal delivery of insulin.
Insulin delivery into the peritoneum is reported to have resulted in a rapid rise in circulating peripheral insulin concentration, which peaked at 30-45 minutes following the initiation of insulin delivery. Furthermore, when the infusion rate of intraperitoneal insulin was reduced to the background rate, a gradual decline in peripheral insulin concentration to normal fasting values resulted. (This free insulin response contrasted to the continuing high levels following subcutaneous insulin injection.) It was, therefore, concluded that normalization of plasma insulin profiles was achievable with intraperitoneal infusion of insulin and, further, that meal-related hyperglycemia (elevated blood glucose) is well-controlled with intraperitoneal insulin and yet hypoglycemic episodes are reduced compared to subcutaneous delivery. For reference, see "Normalization of Plasma Insulin Profiles With Intraperitoneal Insulin Infusion in Diabetic Man," D. S. Schade, R. P. Eaton, N. M. Friedman, and W. J. Spencer, DIABETOLOGIA, 19, 35-39 (1980).
The peritoneum is the largest serous membrane in the body and consists, in the male, of a closed sac, a part of which is applied against the abdominal parietes, while the remainder is reflected over the contained viscera. In the female, the peritoneum is not a closed sac, since the free ends of the uterine tubes open directly into the peritoneal cavity. The part which lines the abdominal wall is named the parietal peritoneum and that which is reflected over the contained viscera constitutes the visceral peritoneum. The space between the parietal and visceral layers of the peritoneum is named the peritoneal cavity. However, under normal conditions, this cavity is merely a potential one, since the parietal and visceral layers are in contact.
For a number of years, it has been well-known that the peritoneal membrane will function fairly effectively as an exchange membrane for various substances. As early as 1923, peritoneal dialysis (an artificial kidney format) was first applied clinically. The first peritoneal access device was a piece of rubber tubing temporarily sutured in place. In 1960, peritoneal dialysis was becoming an established form of artificial kidney therapy and, in order to lessen the discomfort of repeated, temporary punctures into the peritoneal cavity, various access devices permitting the painless insertion of the acute or temporary peritoneal catheters were developed.
The most common peritoneal access device is of the Tenckhoff type: a capped percutaneous (through the skin) silastic tube passes through the abdominal wall into the peritoneal cavity.
Another peritoneal access device (the "Gottloib" prosthesis) consists of a short, "golf tee" design that is adapted to be placed under the skin with a hollow tubular portion extending just into the peritoneal cavity. This device is designed specifically to allow the insertion of an acute peritoneal catheter (a Trocath) through the skin and down through this access tubing directly into the peritoneal cavity. Another device consists of a catheter buried underneath the skin and extending into the peritoneal cavity via a long tubing. Peritoneal dialysis is performed by inserting a large needle into the subcutaneous portion of the catheter.
All of the devices known were designed with one purpose in view: peritoneal dialysis, and are used almost exclusively by one group of patients, those with End-Stage Renal Disease (ESRD), whose kidney function will never return. In simple terms, therefore, the access devices to the peritoneal cavity plus the peritoneal cavity itself constitute an artificial kidney.
A variety of drugs or other fluids are frequently added to the large volumes of peritoneal dialysis solutions and are thus instilled (injected) into the peritoneal cavity for various therapeutic reasons. Some examples of these drugs are antibiotics, amino acids, and insulin (for diabetics). However, such therapeutic maneuvers are fortuitous in that the clinician is simply taking advantage of a particular situation, that is, a peritoneal access device emplaced in a particular group of patients.
In spite of the foregoing, there are cogent reasons for not using existing, permanent peritoneal accesss devices for simple drug injections in a wide variety of patients not suffering ESRD. Most of these devices have what might be termed a relatively large internal volume, that is, it would require anywhere between about five and twenty milliliters, (depending upon the device), to fill the device with fluid. This volume which is a dead volume or dead space, is a very real hindrance in that the injected fluid may simply remain within the device itself instead of entering the peritoneal cavity.
In view of the foregoing, it would be an advancement in the art to provide a novel subcutaneous peritoneal injection catheter which may be readily implanted underneath the skin and provide direct access into the peritoneal cavity. It would also be an advancement in the art to provide a subcutaneous peritoneal injection catheter having a relatively small internal volume while providing a relatively enlarged target area. Such a novel subcutaneous peritoneal injection catheter apparatus and method is disclosed and claimed herein.